In most IBD colon samples we found LMa1 and LMa5 to be highly expressed around UACL that are morphologically and functionally different from the normal colonic crypts. UACL are characterized by defined expression patterns of TFF and mucin molecules and we indeed observed this unusual molecular composition of UACL supporting the notion that they participate to repair processes as strengthened previously in the literature. We also found modifications in the expression of transcription factors that play a role in cell fate decision such as Sox9, Pdx1 and Cdx2 which is in accordance to the changes in the pattern of cellular differentiation documented in human IBD. To date, the physiological relevance of this observation remains unclear. We wondered why and how IBD glands are overexpressing LMa1 and LMa5 and we found that interestingly they also expressed nuclear p53. During the ulceration process, cellular stress and DNA damage occur that typically trigger a p53 response in order to guarantee genome integrity. It is known that active p53 induces a transient cell cycle arrest enabling the cell to activate enzymatic DNA repair systems. In this context, we investigated expression of genes implicated in p53 linked DNA repair such as 53BP1, Mlh1, Msh2 and cH2AX. The first three proteins were expressed in UACL and neighboring glands reflecting a normal response to inflammation and confirming a functional role of nuclear p53 in IBD, while cH2AX was not increased indicative of the absence of DNA double strand lesions. Besides its role in cell cycle regulation and DNA repair, we suggest a novel function of p53 during IBD by modifying BM properties. Our results suggest that p53 triggers LMa1 expression by binding to the promoter. This finding does not exclude the possibility that p53 potentially cooperates with other transcriptional regulators such as SP1 that by itself has been shown to induce the murine lama1 gene. One can postulate that LMa1 could have an indirect positive impact on BM formation by triggering expression of other BM molecules at least in vivo. Indeed our present data showed that LMa5 upregulation was independent of p53 and we previously demonstrated that exogenous expression of LMa1 in grafted intestinal HT29 cells had caused increased expression of LMa5. The concomitant increased of integrin a6b4 would argue for a fortified interaction of colonic epithelial cells with their BM. Yet, although LM-111 and LM-511 have been shown to form independent networks under physiological conditions, their possible connections and timing of assembly into the BM in IBD and associated-cancer will need to be addressed in the future. Upon dysregulated ulceration/repair cycles and acquisition of oncogenic alterations, IBD could R428 abmole degenerate into cancer. To mimic IBD-associated cancer we developed two models of colitisassociated tumorigenesis in transgenic LM-overexpressing mice.